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Apoptosis in human atherosclerotic plaques
F D Kolodgie1, J Narula, P Guillo
1Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20036, USA.
Apoptosis : an International Journal on Programmed Cell Death
|November 25, 2003
Summary
Programmed cell death, or apoptosis, is observed in advanced atherosclerosis. Its role in plaque progression and stability, potentially influencing acute coronary syndromes, is under investigation.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
Background:
- Intimal cell death is a known characteristic of advanced atherosclerotic disease.
- Recent studies indicate that atheroma cells undergo programmed cell death (apoptosis).
Purpose of the Study:
- To explore the pathophysiologic relevance of apoptosis in atherosclerotic disease progression and plaque stability.
- To investigate the cellular components and potential signaling pathways involved in atheroma apoptosis.
Main Methods:
- Utilized DNA in situ end labeling and ultrastructural techniques to identify and study apoptotic cells.
- Examined the types of cells undergoing apoptosis (macrophages, smooth muscle cells, T-cells) and their distribution within lesions.
Main Results:
- Apoptosis may impact lesion progression, potentially reducing plaque burden.
- Apoptosis could contribute to plaque stability by converting cellular lesions to fibrous plaques, or conversely, weaken the fibrous cap, leading to plaque rupture.
- Immune cytokines and tumor suppressor genes (p105RB, p53) are implicated in apoptotic signaling pathways.
Conclusions:
- The precise role and mechanisms of apoptosis in atherosclerosis and acute coronary syndromes require further investigation.
- Apoptosis represents a key cellular process with significant implications for the development and outcomes of atherosclerotic cardiovascular disease.